4.4 Review

Potential therapeutic strategies for myocardial infarction: the role of Toll-like receptors

期刊

IMMUNOLOGIC RESEARCH
卷 70, 期 5, 页码 607-623

出版社

SPRINGER
DOI: 10.1007/s12026-022-09290-z

关键词

Cardiovascular diseases; Myocardial infarction; Pathophysiology; Toll-like receptors; Biomarkers

资金

  1. National Natural Science Foundation of China [81670311]
  2. Natural Science Foundation of Henan Province [182300410010]

向作者/读者索取更多资源

Myocardial infarction is a life-threatening condition with a high incidence and mortality rate worldwide. Understanding the genetic and epigenetic factors involved in its development is crucial for early management and treatment. Toll-like receptors (TLRs) play a role in both adaptive and innate immunity, and their prolonged activation can lead to inflammation and contribute to the development of myocardial inflammation, MI, ischemia-reperfusion injury, myocarditis, and heart failure.
Myocardial infarction (MI) is a life-threatening condition among patients with cardiovascular diseases. MI increases the risk of stroke and heart failure and is a leading cause of morbidity and mortality worldwide. Several genetic and epigenetic factors contribute to the development of MI, suggesting that further understanding of the pathomechanism of MI might help in the early management and treatment of this disease. Toll-like receptors (TLRs) are well-known members of the pattern recognition receptor (PRR) family and contribute to both adaptive and innate immunity. Collectively, studies suggest that TLRs have a cardioprotective effect. However, prolonged TLR activation in the response to signals generated by damage-associated molecular patterns (DAMPs) results in the release of inflammatory cytokines and contributes to the development and exacerbation of myocardial inflammation, MI, ischemia-reperfusion injury, myocarditis, and heart failure. The objective of this review is to discuss and summarize the association of TLRs with MI, highlighting their therapeutic potential for the development of advanced TLR-targeted therapies for MI.

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